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G Levi

Publications and source records attributed to G Levi.

At least 19 recordsLinked to original sources
PubMed1992

Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha.

Astrocyte-enriched populations were established from human embryonic brain analyzed for their ability to synthesize cytokines potentially relevant for mechanisms of inflammation and immunity in the brain. Unstimulated astrocytes did not secrete significant IL-6, IL-8, macrophage CSF (M-CSF), granulocyte-macrophage CSF (GM-CSF), or granulocyte-CSF (G-CSF), as determined by specific ELISA and/or bioassay. With the exception of M-CSF mRNA, transcripts for the above factors were not detected in unstimulated astrocytes. On exposure of human astrocytes to IL-1 beta, high levels of IL-6, IL-8, M-CSF, G-CSF, and GM-CSF mRNAs were detected; moreover, active secretion of all the above cytokines was demonstrated. TNF-alpha was also able to stimulate IL-6, IL-8, M-CSF, GM-CSF, and G-CSF synthesis and secretion, but was generally less potent than IL-1 beta. No IL-3 mRNA or protein was detected in unstimulated or cytokine-treated astrocytes. IL-1 alpha and IL-1 beta mRNAs and proteins were not detected in unstimulated astrocytes, but were present in very small amounts after stimulation with TNF-alpha/IL-1 beta. No IL-6, M-CSF, GM-CSF, G-CSF, or IL-8 were induced by IL-1 beta or TNF-alpha in early primary cultures, which mainly contain undifferentiated neuronal/glial progenitor cells. These studies demonstrate for the first time the production of multiple cytokines by normal human astrocytes stimulated in culture by IL-1 beta and TNF-alpha. The capacity of human astrocytes to synthesize and release cytokines active on hemolymphopoietic cells supports the concept that these cells play an important role in the regulation of inflammatory and immune responses in a variety of brain pathologies.

Astrocytes↗
PubMed1992

Paraganglioma of the inferior laryngeal paraganglia. A case report.

Laryngeal paragangliomas are uncommon, usually benign neoplasms. The overwhelming majority of these tumors are supraglottic, arising from the superior laryngeal parasympathetic paraganglia. Few paragangliomas of the infraglottic region have been described. We describe the case of a 35-year-old man with a family history of carotid body tumors who presented with an infraglottic paraganglioma.

Adult↗
PubMed1992

Developmental appearance, antigenic profile, and proliferation of glial cells of the human embryonic spinal cord: an immunocytochemical study using dissociated cultured cells.

We have investigated the time of appearance of the earliest differentiating glial cell types of human spinal cord using a panel of antigenic markers to identify them in cultures from 6- to 9-week-old human embryos. Immunolabeling performed at 14 h in vitro with the O4 mAb, an early oligodendrocyte marker, showed the presence of oligodendrocytes during the 7th week of age. At 8 weeks only a few of the O4+ cells expressed galactocerebroside (GalC), a marker of more differentiated oligodendrocytes. All the O4+ and GalC+ cells were vimentin+ and some of the GalC+ cells were A2B5+, GD3+ and SSEA-1+. During the first week in vitro many of the O4+ cells exhibiting a more immature, bi- or tri-polar morphology incorporated [3H]thymidine into their nuclei. Cells expressing the astrocyte-specific marker GFAP could be first observed at 8 weeks; almost all of these GFAP+ cells, which should correspond to radial glia on the basis of the current literature, were vimentin+, A2B5+, GD3+, and SSEA-1+. At 2 days in vitro incorporation of [3H]thymidine could be shown in a small fraction of these cells. The finding that radial glia and oligodendrocytes expressed similar antigenic features and the additional observation that a small, but consistent fraction of the cells were simultaneously labeled by O4 and anti-GFAP antibodies support the hypothesis that, in the human spinal cord, radial glial cells can give rise to both oligodendrocytes and astrocytes; in this respect, radial glial cells may be similar to the A2B5+, GD3+, vimentin+ bipotential glial progenitors previously identified in cultures from developing rat CNS, which also express A2B5, GD3, and vimentin.

Antibodies↗
PubMed1992

Astrocyte cultures from human embryonic brain: characterization and modulation of surface molecules by inflammatory cytokines.

Astrocyte-enriched cultures were established upon passaging of primary cultures from the myelencephalon and mesencephalon of 7-9-week-old human embryos. Immunocytochemical analysis showed that third-fourth passage cultures were composed of a highly enriched population of proliferating, epithelioid cells, up to 90% of which expressed glial fibrillary acidic protein (GFAP); no macrophages and very few fibroblasts (less than 2%) were present. GFAP expression and proliferation declined upon further culturing in serum-containing medium but could be transiently reinduced by growing the cells in a serum-free chemically defined medium. Large numbers of GFAP+ astrocytes were obtained from each embryo and could be stored frozen and recultured. Using flow cytometric analysis, human astrocyte cultures were examined for basal and cytokine [interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha)]-induced expression of molecules that may be involved in astrocyte-T-lymphocyte interactions. Cultured human astrocytes spontaneously expressed major histocompatibility complex (MHC) class I antigens and variable levels of MHC class II; MHC class I levels were increased upon IFN-gamma and TNF-alpha treatment, whereas MHC class II antigens were induced on most of the astrocytes by IFN-gamma. Among the molecules involved in antigen-independent interactions between T lymphocytes and target cells, lymphocyte function-associated molecule-3 (LFA-3) was spontaneously expressed by most cultured human astrocytes, whereas intercellular adhesion molecule-1 (ICAM-1) was present at variable levels in non-stimulated astrocytes and was greatly induced by IFN-gamma, TNF-alpha, and IL-1 beta. In this study we also show that the above cytokines upregulate astroglial expression of adhesion molecules of the integrin family (VLA-1, VLA-2, and VLA-6) that may be involved in astrocyte-extracellular matrix interaction and play a role in the astrocyte reactive changes occurring at sites of brain injury and inflammation. The human astrocyte cultures developed here represent a useful in vitro model to further investigate mechanisms involved in bidirectional communication between central glia and cells of the immune system.

Astrocytes↗
PubMed1992

Depression by sodium ions of calcium uptake mediated by non-N-methyl-D-aspartate receptors in cultured cerebellar neurons and correlation with evoked D-[3H]aspartate release.

In a previous study we noted that the release of D-[3H]aspartate evoked by non-N-methyl-D-aspartate (non-NMDA) receptor agonists in cultured rat cerebellar granule cells was enhanced in the absence of extracellular Na+. To explain this apparent paradox, we tried in the present investigation to correlate the effect of Na+ removal on the kainate (KA)- and quisqualate (QA)-induced D-[3H]aspartate release with that on KA- and QA-induced 45Ca2+ accumulation. The releasing activity of KA, which was only partially Ca2+ dependent in the presence of Na+, became totally Ca2+ dependent in its absence. Moreover, the releasing activity of QA, which was Ca2+ independent in the presence of Na+, became 50% Ca2+ dependent in the absence of the monovalent cation. The releasing action of both agonists was in all cases antagonized by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and that induced by KA was also sensitive to kynurenic acid. When glutamate was tested as an agonist in the presence of Na+, it was found that its D-[3H]aspartate releasing action was Ca2+ independent and was largely due to heteroexchange. The evoked release was Ca2+ independent, scarcely sensitive to CNQX, and insensitive to NMDA antagonists. In Na(+)-free medium, the glutamate-evoked D-[3H]aspartate release was lower (due to the abolishment of heteroexchange), but was totally Ca2+ dependent and antagonized by CNQX and kynurenate. KA (30 microM-1 mM) stimulated the accumulation of 45Ca2+ in a dose-dependent and CNQX-sensitive way, the effect being progressively higher as the Na+ concentration in the medium was decreased. Li+ affected KA-induced 45Ca2+ accumulation in a way similar to Na+, although 45Ca2+ uptake was somewhat lower in Li(+)-containing medium. The voltage-activated calcium channel antagonists La3+ and (-)-202-791 caused only a limited inhibition of the KA-induced 45Ca2+ influx both in the presence and in the absence of Na+. Under all the conditions tested [presence and absence of Na+ and of (-)-202-791], the kainate-induced 45Ca2+ uptake was scarcely sensitive to the NMDA antagonist 2-amino-5-phosphonovalerate. QA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid also stimulated 45Ca2+ influx in a CNQX-sensitive way, the effect being enhanced in Na(+)-free media. These agonists were, however, less effective than KA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Astrocyte heterogeneity: endogenous amino acid levels and release evoked by non-N-methyl-D-aspartate receptor agonists and by potassium-induced swelling in type-1 and type-2 astrocytes.

The aim of the present study was to determine whether endogenous amino acids are released from type-1 and type-2 astrocytes following non-N-methyl-D-aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in type-1 or type-2 astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in type-1 than in type-2 astrocytes. (b) The spontaneous release of glutamine and taurine was higher in type-1 than in type-2 astrocytes; that of other amino acids was similar. (c) Exposure of type-2 astrocyte cultures to 50 microM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of type-1 astrocyte cultures to 50-200 microM kainate or 50 microM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of type-1 or type-2 astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine greater than glutamate greater than aspartate. The effect was somewhat more pronounced in type-2 than in type-1 astrocytes. Veratridine (50 microM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high [K+] appeared to be related to cell swelling, in both type-1 and type-2 astrocytes. Swelling and K(+)-induced release were somewhat higher in type-2 than in type-1 astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non-NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from type-2 but not from type-1 astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both type-1 and type-2 astrocytes. The absence of kainate- and quisqualate-evoked release in type-1 astrocytes suggests that the density of non-NMDA receptors in this cell type is very low.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Ventrolateral regionalization of Xenopus laevis mesoderm is characterized by the expression of alpha-smooth muscle actin.

Mesodermal patterning in the amphibian embryo has been extensively studied in its dorsal aspects, whereas little is known regarding its ventrolateral regionalization due to a lack of specific molecular markers for derivatives of this type of mesoderm. Since smooth muscles (SM) are thought to arise from lateral plate mesoderm, we have analyzed the expression of an alpha-actin isoform specific for SM with regard to mesoderm patterning. Using an antibody directed against alpha-SM actin that recognized specifically this actin isoform in Xenopus, we have found that the expression of alpha-SM actin is restricted to visceral and vascular SM with a transient expression in the heart. The overall expression of the alpha-SM actin appears restricted to the ventral aspects of the differentiating embryo. alpha-SM actin expression appears to be activated following mesoderm induction in animal cap derivatives. Moreover, at the gastrula stage, SM precursor cells are regionalized since they will only differentiate from ventrolateral marginal zone explants. Using the animal cap assay, we have found that alpha-SM actin expression is specifically induced in treated animal cap with bFGF or a low concentration of XTC-MIF, which induce ventral structures, but not with a high concentration of XTC-MIF, which induces dorsal structures. Altogether, these results establish that alpha-SM actin is a reliable marker for ventrolateral mesoderm. We discuss the importance of this novel marker in studying mesoderm regionalization.

Actins↗
PubMed1992

[Adhesion and mobility of embryonic and tumoral cells].

Regulation of a number of adhesion molecules during neural crest cell migration was studied. The neural crest, a transient embryonic neural epithelium structure, undergoes mesenchymal transformation (epithelial-mesenchymal transition). The cells then migrate, giving rise to a variety of elements including the peripheral nervous system and melanocytes. During migration, neural crest cells do not express functional cell Adhesion Molecules but interact specifically with cell-binding domains in fibronectin molecules. A rat bladder carcinoma cell line was used as an in vitro model to study conversion of epithelial cells to a migratory fibroblast-like state. Conversion can be induced by culture on collagen or exposure to acidic Fibroblast Growth Factor (aFGF). Furthermore, constitutive fibroblast-like transformation can be induced by transfection with cDNA encoding aFGF. Growth factor-producing clones exhibit increased invasive and metastatic properties as compared with non-FGF-producing control cells. This model may provide increased understanding of the role of the different adhesion molecules in processes involving cell remodeling, such as tumor spread and development of metastases.

Cadherins↗
PubMed1992

Neurobiological aspects of glial cells: astrocyte subtypes and the 0-2A glial cell lineage.

Cell culture studies have shown the existence, in the rat CNS, of two populations of astrocytes, generally named type-1 and type-2 astrocytes, differing in a number of morphological, antigenic and functional features, and belonging to two different cell lineages. Type-2 astrocytes seem to derive from a bipotential glial progenitor cell (0-2A progenitor) which gives rise also to oligodendrocytes. Several epigenetic factors influence the proliferation and the differentiation destiny of 0-2A progenitors. Among such factors, heterotypic and homotypic glial cell interactions appear to be particularly important. Interaction with factors present on the surface of type-1 astrocytes or in their extracellular matrix leads to an increased proliferation of 0-2A progenitors and facilitates their oligodendroglial differentiation, while homotypic interactions among the progenitors induce them to differentiate into oligodendrocytes through the secretion of autocrine non mitogenic factors.

Animals↗
PubMed1992

Study of the function and regulation of liver N-CAM in Xenopus laevis.

The liver of Xenopus laevis is a unique exception in terms of the cell adhesion molecules (CAM) which it expresses. In most species, hepatocytes are characterized by the expression of the epithelial Ca(2+)-dependent CAM E-cadherin or of closely related variants of this molecule (e.g., L-CAM); in Xenopus liver, however, the levels of expression of epithelial cadherins is very low while a thyroxine-inducible isoform of N-CAM is expressed in postmetamorphic hepatocytes. Since Xenopus liver N-CAM is localized in regions of contact between hepatocytes, it has been proposed that it might be involved in mediating hepatocyte adhesion in this species. In this study, we demonstrate that N-CAM can indeed act as a functional adhesion molecule in the liver of Xenopus and that its expression is correlated with a number of profound morphological changes of this organ. After thyroxine treatment, hepatocytes are no longer organized in long loose cords but in compact lobules of cells. Furthermore, at the ultrastructural level, plasma membranes are in much closer proximity with the appearance of electron-dense material in areas of closer contact. We have established two novel culture systems for premetamorphic Xenopus hepatocytes as adherent and non-adherent cells, and we describe the induction of expression of N-CAM in these cells. Given the difference in the profile of adhesion molecules present in the liver of Xenopus and of other species, our results are discussed in view of the importance of the expression of a specific set of cell adhesion molecules in defining the development of homologous organs in different species.

Animals↗
PubMed1992

Right ventricular diastolic function in chronic obstructive lung disease.

Early detection of diastolic dysfunction in chronic obstructive lung disease (COLD) patients could have great prognostic value. Echocardiography has been shown to be a useful technique in studying left ventricular diastolic function. A noninvasive method of studying right ventricular diastolic function has not yet been reported. Pulsed Doppler echocardiography was used to assess right ventricular diastolic function in three groups of subjects: Group I: 35 COLD patients with pulmonary hypertension; Group II: 32 COLD patients without pulmonary hypertension; and Group III: 18 control subjects. Ratios between peak atrial filling velocity (A) and peak early filling velocity (E) (A/E), deceleration half times of the right ventricular rapid filling wave (DHT), and the interval between pulmonary valve closure and tricuspid valve opening (isovolumic relaxation times) (Pc-To) were significantly different in Group I in comparison to Groups II and III. Sensitivity of A/E ratio and Pc-To were 82 and 77%, respectively, and specificity 90 and 72%, respectively; positive predictive values were 90 and 75%, respectively, and negative predictive value 82 and 74% respectively. The multiple correlation coefficient between A/E, acceleration time (ACT), DHT, Pc-To and mean pulmonary artery pressure was 0.75 for Groups I and II together. In conclusion 2D echo-Doppler proved to be useful in evaluating right ventricular diastolic function in all hypertensive COLD patients, revealing a high correlation between diastolic parameters and mean pulmonary artery pressure in both normotensive and hypertensive COLD patients.

Echocardiography, Doppler↗
PubMed1991

Is the oligodendroglial differentiation of bipotential oligodendrocyte-type 2 astrocyte progenitors promoted by autocrine factors?

When immature O-2A (oligodendrocyte-type 2 astrocyte) lineage cells purified from rat mixed cortical glial cultures were subcultured at low density in 10% fetal calf serum (FCS)-containing medium they largely differentiated into type-2 astrocytes. When the same number of cells was subcultured at high density in the same volume of medium the proportion of O-2A progenitors differentiating into oligodendrocytes was substantially increased. The possibility that oligodendrocyte differentiation in high-density cultures is facilitated by autocrine factors is supported by the observation that a medium conditioned by high-density subcultures of purified O-2A cells contains high molecular weight (greater than 30 kDa), non-mitogenic factor(s) capable of inducing a rapid differentiation of immature 0-2A cells into oligodendrocytes even in low-density cultures.

Animals↗
PubMed1991

Purification and partial characterization of Xenopus laevis tenascin from the XTC cell line.

We report here the purification of tenascin, an extracellular matrix molecule involved in the control of morphogenesis, from the conditioned medium of the Xenopus XTC cell line. Tenascin was purified by affinity chromatography on a column of the monoclonal antibody mAb TnM1; the molecule eluted from this column has a relative molecular mass of 210 kDa after reduction. Electrophoretic analysis under non-reducing conditions shows that the purified components are oligomeric disulfide-linked complexes which barely enter a 4% polyacrylamide gel. Upon rotary shadowing these molecules appear to possess a central globular domain to which pairs or triplets of arms are attached. Polyclonal antibodies have been raised against purified Xenopus tenascin. They recognise specifically the antigen on Western blots of XTC conditioned medium and adult brain, by immunofluorescence, these antibodies reveal large amounts of tenascin in the secretory vesicles as well as in the extracellular matrix of XTC cells. In the Xenopus tadpole, they stain the developing cartilage, the basal lamina of skin epidermis, myotendinous ligaments and restricted regions of the central nervous system.

Animals↗
PubMed1991

GABA release triggered by the activation of neuron-like non-NMDA receptors in cultured type 2 astrocytes is carrier-mediated.

Kainate (KA), quisqualate (QA), and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) stimulated gamma-aminobutyric acid [3H]gamma-aminobutyric acid (GABA) release from cultured cerebellar type 2 astrocytes and from their bipotential precursors. The evoked release was prevented by the antagonist 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline (CNQX). AMPA and QA applied together with KA at concentrations around or above their EC50S (20-50 microM) antagonized the stimulatory effect of KA on [3H]GABA release. On the other hand, the releasing action of KA was potentiated by concentrations of QA in the low micromolar range (2-5 microM), particularly when the concentration of KA was at the borderline of effectiveness (10 microM). KA and QA did not elevate intracellular cyclic GMP levels in astrocyte cultures, although guanylate cyclase was present in both type 2 and type 1 astrocytes. The inability of KA to elevate cyclic GMP levels in astrocytes was the only major difference in the behavior of this glutamate agonist between astroglial and neuronal cultures. The GABA transport inhibitor nipecotic acid or replacement of NaCl with LiCl abolished [3H]GABA uptake and also KA- and QA-induced release of preaccumulated [3H]GABA. Therefore, [3H]GABA was released from type 2 astrocytes and their progenitors through its Na(+)-dependent transport system, operating in an outward direction when the cells were depolarized by non-NMDA receptor agonists.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

Heterotypic and homotypic cellular interactions influencing the growth and differentiation of bipotential oligodendrocyte-type-2 astrocyte progenitors in culture.

Cell populations highly enriched in oligodendrocyte-type-2 astrocyte (O-2A) progenitors (so defined by their ability to bind the monoclonal antibodies LB1 and O4, and by the lack of expression of the differentiated glial markers galactocerebroside and glial fibrillary acidic protein (GFAP) were obtained from rat mixed cortical glial cultures. The O-2A progenitors were grown at low density (2 X 10(4) cells/cm2) in BME + 10% fetal calf serum (FCS) on a poly-L-lysine (PLL) substrate (controls) or on a substrate of purified type-1 astrocytes (AS) killed by air drying (K-AS), in order to analyze the effects of the interaction between the two cell types on the growth and differentiation of the immature O-2A cells, independently of the mitogenic soluble factors (e.g., platelet-derived growth factor; see Raff, 1989, Science 243, 1450-1455) secreted by type-1 AS. While on PLL most of the progenitors differentiated into GFAP+ type-2 AS within 1 week, on K-AS they largely differentiated into GalC+ oligodendrocytes (OL). On the latter substrate, however, the precursors achieved a higher density, due to higher proliferative activity. The additional observation, that when immature O-2A cells were seeded at high density (greater than 5 X 10(4) cells/cm2) on PLL their differentiation into OL was much more pronounced than in cultures of lower density, indicates that there is a close correlation between the density of immature O-2A cells and lineage decision, and that the increased OL differentiation of the immature O-2A cells on K-AS is at least partly related to the higher density achieved by the cells on this substrate. The enhanced proliferation of immature O-2A cells on K-AS did not appear to be related to platelet-derived growth factor or fibroblast growth factor remaining attached to the substrate, nor to known components of the extracellular matrix (ECM), such as heparan sulfate, chondroitin sulfate, laminin, or fibronectin, but was probably due to other components of a polypeptide nature present in the ECM produced by type-1 AS. A cell-free ECM was in fact almost as mitogenic as the K-AS substrate, and the mitogenic activities of both K-AS and AS-ECM were similarly inhibited by a set of enzymatic (pronase, trypsin) and physicochemical (heat, pH) treatments.

Animals↗
PubMed1991

Release of endogenous and newly synthesized glutamate and of other amino acids induced by non-N-methyl-D-aspartate receptor activation in cerebellar granule cell cultures.

Amino acid release studies were performed by an HPLC procedure using differentiated rat cerebellar granule cell cultures. Kainic acid (KA; 50 microM) caused an increase (about threefold) in the release of endogenous glutamate and a lesser, but statistically significant, increase in the release of glutamine, glycine, threonine, taurine, and alanine. Quisqualic acid (QA) and, to a lesser degree, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) (both 50 microM) enhanced the release of the following amino acids in the order glutamate greater than aspartate greater than or equal to taurine, whereas the release of other amino acids was either unaffected or affected in a statistically nonsignificant way. The release of glutamate induced by KA was partially (43%) Ca2+ dependent. The other release-inducing effects of KA and QA were not Ca2+ dependent. In all cases, the evoked release could be prevented by the non-N-methyl-D-aspartate (non-NMDA) receptor antagonist 6-cyano-2,3-hydroxy-7-nitroquinoxaline, and thus appeared to be receptor mediated. NMDA (5 and 50 microM) had no release-inducing activity. The KA-, QA-, and AMPA-evoked release of newly synthesized [3H]glutamate and [3H]aspartate (formed in the cells exposed to [3H]glutamine) was very similar to the evoked release of endogenous glutamate and aspartate. On the other hand, the release of preloaded D-[3H]aspartate (purified by HPLC in the various fractions analyzed, before radioactivity determination) induced by 50 microM KA was twice as high as that of endogenous glutamate. In the case of high [K+] depolarization, in contrast, the release of preloaded D-[3H]aspartate was approximately 30% lower than that of endogenous glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗